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光皮肤病学中皮肤疾病机制的证据与推测

Evidence and conjecture about mechanisms of cutaneous disease in photodermatology.

作者信息

Porter Rebecca M, Anstey Alex

机构信息

Royal Gwent Hospital, Aneurin Bevan University Health Board, Newport, UK.

出版信息

Exp Dermatol. 2014 Aug;23(8):543-6. doi: 10.1111/exd.12467.

Abstract

Photosensitivity disorders are caused by a variety of mechanisms. Three common themes are as follows: excess chromophore allowing visible light energy to cause photodynamic damage, reduced DNA repair capacity to UV-induced DNA damage, and enhanced sensitivity to light-induced allergens mediated immunologically. Although the cause of each condition may be known, the precise pathogenesis underlying the photosensitivity has taken longer to understand. By focussing on three clinical disorders under each of these themes, we have explored the following: why erythropoietic protoporphyria differs so markedly from the other cutaneous porphyrias; how a DNA repair defect was eventually revealed to be the underlying cause of the vitamin B3 deficiency disorder of pellagra; an immunological explanation for the over reactivity to photoallergens in chronic actinic dermatitis.

摘要

光敏性疾病由多种机制引起。三个常见主题如下:发色团过量使得可见光能量导致光动力损伤、紫外线诱导的DNA损伤的DNA修复能力降低,以及对光诱导变应原介导的免疫反应增强。尽管每种病症的病因可能已知,但光敏性背后的确切发病机制却需要更长时间才能理解。通过关注这些主题下的三种临床病症,我们探讨了以下内容:为什么红细胞生成性原卟啉症与其他皮肤卟啉症有如此明显的差异;DNA修复缺陷最终如何被揭示为糙皮病维生素B3缺乏症的根本原因;对慢性光化性皮炎中光变应原过度反应的免疫学解释。

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